Congestive heart failure is a major issues for cardiologists and to fully understand heart failure, it is important to understand the mechanism of the development of cardiac hypertrophy. Hemodynamic overload, namely mechanical stress, is a major cause of cardiac hypertrophy and to dissect the signaling pathways from mechanical stress to cardiac hypertrophy, an in-vitro device by which mechanical stress can be imposed on cardiac myocytes of neonatal rats cultured in serum-free conditions has been developed. Passively stretching cardiac myocytes cultured on silicone membranes induced various hypertrophic responses, such as activation of the phosphorylation cascades of many protein kinases, expression of specific genes and an increase in protein synthesis. During this process, secretion and production of vasoactive peptides, such as angiotensin II and endothelin-1, were increased and they played critical roles in the induction of these hypertrophic responses. Candidates for the `mechanoreceptor' that receives the mechanical stress and converts it into intracellular biochemical signals have been recently demonstrated. Gene therapy and cell transplantation are hopeful strategies for the treatment of heart failure and require an understanding of how normal cardiac myocytes are differentiated. A key gene that plays a critical role in cardiac development has been isolated. The cardiac homeobox-containing gene Csx is expressed in the heart and the heart progenitor cells from the very early developmental stage, and targeted disruption of the murine Csx results in embryonic lethality because of the abnormal looping morphogenesis of the primary heart tube. With a cardiac zinc finger protein GATA4, Csx induces cardiomyocyte differentiation of teratocarcinoma cells as well as upregulation of cardiac genes. Mutations of human CSX cause various congenital heart diseases including atrial septal defect, ventricular septal defect, tricuspid valve abnormalities and atrioventricular block. (Jpn Circ J 2001; 65: 353 - 358)

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Between 1973 and 1998, 263 patients with acute aortic dissection were medically treated only. They were divided into 4 groups: Stanford type A and B with open false lumen (open) or with early thrombosed false lumen (thrombosed). An event was defined as death by dissection or re-dissection. Gender, age, maximum diameter of dissected aorta and presence of shock at onset were examined as risk factors. In the open false lumen group, the presence of shock was associated with the event. During the chronic period, the diameter of the aorta was associated with prognosis in open type B dissection. The rate of event was higher in the open type A and B groups than in the thrombosed type A and B groups; however, there was no difference in the event-free rate between types A and B in patients surviving the acute period. The prognosis of medically treated dissecting aorta was not poor in patients with type B or with early thrombosed false lumen. The presence of shock at onset with open false lumen and the diameter of the aorta (≥40 mm) in type B were significantly correlated with a poor prognosis. (Jpn Circ J 2001; 65: 359 - 363)

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The present study examined the Doppler echocardiograms of 742 patients with an outlet ventricular septal defect (VSD) who were seen at the National Cardiovascular Center from 1987 to 1999. Of these, 450 patients were followed for longer than 1 year; 161 of these 450 were younger than 12 months when first examined. During follow-up, Doppler echocardiographic examination was repeated at least once a year. The medical charts of these patients were reviewed. Doppler echocardiographic findings were analysed in patients whose defect closed spontaneously:spontaneous closure at the age of 1-25 years was identified in 17 (3.8%) of 450 patients who were followed for longer than 1 year, and 7 (4.3%) of the 161 patients who were younger than 12 months at the first examination. All closed VSDs were originally smaller than 4 mm. Although 5 cases of 17 developed trivial deformity of the right coronary cusp, suggesting a prolapse, this did not progress. Of these 5, trivial aortic regurgitation (AR) was detected in one patient, while another patient in the group of 17 developed trivial AR without any deformity of the right coronary cusp. Aortic regurgitation was not progressive in either patient. An outlet VSD closes spontaneously in a small percentage of patients without developing progressive AR. (Jpn Circ J 2001; 65: 364 - 366)

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Electrophysiological findings suggest that concealed anterograde conduction through accessory pathways may exist even during sinus rhythm in patients with so-called concealed Wolff-Parkinson-White (WPW) syndrome. To evaluate the pre-excitation characteristics in various types of WPW syndrome, high-resolution electrocardiograms were analyzed in 81 consecutive WPW syndrome patients and 50 age-matched normal subjects. The WPW group consisted of 30 cases of concealed WPW diagnosed by electrophysiological study, 38 cases of manifest WPW in which apparent delta waves were constant, and 13 cases of intermittent WPW in which the delta waves appeared periodically. The duration of the low-amplitude, high-frequency components of the signal-averaged filtered QRS complex that preceded the earliest upstroke of the surface QRS, including any delta waves (preceding potential duration, PPD), and the duration of low amplitude signals less than 10 μV (I-LAS10) or 20 μV (I-LAS20) were measured as parameters of pre-excitation. The PPDs in concealed and intermittent WPW were both significantly longer than in manifest WPW or in control subjects (6.8±2.7 ms, 7.9±3.5 ms vs 2.3 ±3.2 ms, 1.0±1.6 ms, both p<0.0001). Abnormally prolonged PPDs (>4 ms) were observed in 90% of concealed WPW cases and 76.9% of intermittent WPW, but in only 4% of normal subjects and 31.6% of manifest WPW. Both I-LAS10 and I-LAS20 in the 3 types of WPW syndrome were significantly longer than in normal subjects. The initial portion of the filtered QRS in concealed WPW closely resembled that of intermittent WPW. These results strongly suggest that in concealed WPW anterograde conduction through accessory pathways does occur and produces small amounts of pre-excitation even during sinus rhythm. The study concluded that, despite its name, concealed WPW is not completely concealed, and that non-invasive diagnosis during sinus rhythm is possible by using high-resolution electrocardiography to detect the concealed anterograde pre-excitation. (Jpn Circ J 2001; 65: 367 - 370)

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The athlete's heart is commonly characterized by an increase in left ventricular mass because of an increase in the left ventricular diastolic cavity dimensions or wall thickness or both. Endurance exercise also induces numerous cardiovascular adaptations, including increased vagal tone. However, the sympathetic function has not yet been precisely elucidated, so the present study evaluated cardiac sympathetic nerve function from metaiodobenzylguanidine (MIBG) images obtained 15 and 180 min after the injection of ¹²³I-MIBG at a dose of 111 MBq. The ratio of heart/mediastinum count (H/M) and the washout rates of ¹²³I-MIBG (WR) were calculated in 25 consecutive patients who were athletes (aged 52±13 years) and 23 normal subjects. There was a significant difference in the H/M between the athletic and normal hearts (2.3±0.3 vs 2.6±0.3, p<0.01, Scheffe's test). An increased WR was observed in the athletes group when compared with the normal group (34±4 vs 28±3, p<0.01), and there was a significant correlation between WR and the left ventricular mass index (r=0.578, p<0.01). Prolonged exercise training may alter cardiac sympathetic nerve function, which can be detected by MIBG imaging. (Jpn Circ J 2001; 65: 371 - 374)

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Large left atrium (LA) and LA appendage (LAA) dysfunction are known to relate to cardiogenic thromboembolism, so the present study investigated the relation of the atrial fibrillatory wave (F wave) amplitude to hemostatic markers and LAA function. Transthoracic and transesophageal echocardiographic studies were performed in 82 consecutive patients with chronic, nonrheumatic atrial fibrillation (AF). Patients were divided into 2 groups according to F wave amplitude in lead V₁ on the 12-lead ECG: coarse AF (the greatest amplitude of F wave ≥1 mm, n=44) and fine AF (<1 mm, n=38). Plasma levels of thrombin-antithrombin III complex, D-dimer, platelet factor 4 and β-thromboglobulin were determined. Compared with patients with coarse AF, those with fine AF had lower LAA peak flow velocity (p<0.05) and higher prevalence of embolic cerebral infarction (50% vs 27%, p<0.05). Platelet activity did not differ between the 2 groups; however, plasma levels of thrombin - antithrombin III complex and D-dimer were significantly higher in patients with fine AF than in those with coarse AF (p<0.05). Multiple logistic regression analysis showed that fine AF was independently associated with cerebral embolism. Therefore, the presence of fine F wave in V₁ would be a useful marker of LAA dysfunction and hypercoagulability, and indicate a risk for cerebral embolism in patients with chronic, nonrheumatic AF. (Jpn Circ J 2001; 65: 375 - 380)

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This study was designed to assess the diagnostic accuracy of the percentage of resting systolic wall thickening (WT), dobutamine stress echocardiography (DSE), resting cyclic variation of integrated backscatter (IBS-CV), and low-dose dobutamine stress IBS-CV (DSE-IB) for the prediction of regional function recovery (RFR) in patients with chronic left ventricular (LV) ischemic dysfunction. The study also evaluated whether or not global LV function affected the diagnostic accuracy. All studies were conducted before percutaneous transluminal coronary angioplasty (PTCA) and RFR was assessed after PTCA (mean interval, 10 months) in 30 patients with chronic LV ischemic dysfunction. Patients were divided into 2 groups according to the LV ejection fraction (LVEF): group A, LVEF <40%, n=14; group B, LVEF ≥40%, n=16. Of a total of 480 segments, 37 initially demonstrating akinetic wall motion before PTCA were analyzed. The wall motion of 24 of the 37 segments improved on visual analysis after PTCA. In the prediction of RFR, resting WT, DSE, resting IBS-CV and DSE-IB had sensitivities of 79%, 79%, 92% and 62%, and specificities of 54%, 84%, 83% and 69%, respectively. In particular, the resting IBS-CV in group A, as well as DSE, was an excellent predictor of RFR (sensitivity, 100%; specificity, 86%; vs sensitivity, 82%; specificity, 78%; respectively). Therefore, both resting IBS-CV and DSE are useful predictors for RFR in patients with chronic LV ischemic dysfunction. (Jpn Circ J 2001; 65: 381 - 388)

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The TAMI-6 trial has demonstrated that coronary reperfusion >6 h after onset (ie, late reperfusion) in patients with acute myocardial infarction (AMI) does not improve left ventricular (LV) function during the chronic phase of infarction. However, the low patency rate (only 60%) of the infarct-related artery (IRA) during the chronic phase in the TAMI-6 trial raises a new hypothesis that late reperfusion with a higher patency rate may improve LV function during the chronic phase. Forty-four patients with AMI, who were admitted to hospital 6-24 h after the symptom onset and in whom emergency coronary angiography revealed a total occlusion of the IRA, were randomly assigned to either the late reperfusion group (n=22) or the non-reperfusion group (n=22). The initial success rate of reperfusion therapy in the late reperfusion group was 86% and the chronic patency rate of the IRA was 91%. The improvements in ejection fraction and chord shortening in the infarct region from the acute phase to the chronic phase were significantly greater in the late reperfusion group than in the non-reperfusion group. Late reperfusion with a high patency rate of the IRA significantly improves LV global and regional function in patients with AMI.(Jpn Circ J 2001; 65: 389 - 394)

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Sixteen patients with mild to moderate heart failure were examined to investigate whether sympathetic deactivation plays a role in the improvement in the failing heart by chronic angiotensin converting enzyme (ACE) inhibition. Measurements, including echocardiography, blood examinations, neurohumoral samplings (atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), norepinephrine), and spectral heart rate variability analysis by Holter electrocardiography, were carried out before and 6 months after the administration of lisinopril (5-10 mg/day). Quality of life assessment was accomplished by the Specific Activity Scale (SAS) questionnaire. Treatment with lisinopril for 6 months resulted in a significant reduction in systolic blood pressure. The left ventricular diastolic dimension significantly decreased and fractional shortening significantly increased on echocardiography. Of the 16 patients, 8 had improvement in their symptoms as measured by the SAS. Lisinopril did not significantly reduce the plasma norepinephrine concentration, but there was a significant reduction in the plasma ANP and BNP concentrations. In the heart rate power spectral analysis, total spectral power, high-frequency components and low/high frequency ratios did not change significantly with lisinopril. The mechanism by which ACE inhibitors improve mild to moderate heart failure is not by suppressing sympathetic activity. (Jpn Circ J 2001; 65: 395 - 398)

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The relationship between ventilation (V_E) and CO₂ output (V_CO2) is fitted linearly. The steeper gradient implies excessive ventilation. Through an evaluation of the V_E-V_CO2 slopes, this study investigated whether patients with acute myocardial infarction (AMI) have excessive ventilation and whether it improved in 4 months. The V_E-V _CO2 slopes were determined in exercise tests at 1 and 4 months in 131 patients with AMI. Patients were divided into 3 groups according to the 1 month V_E-V_CO2 slope value: (i) normal (<30); (ii) intermediate (30-32); and (iii) excessive (>32). In the normal group (n=76), at 4 months, the slope decreased in 10, increased in 5 and remained unchanged in 61 patients; in the intermediate (n=31) group, 9, 2 and 20; and in the excessive (n=24) group, 15, 3 and 6, respectively, showing that the slope reduction was greater in the excessive group (p<0.01). The slope correlated with age and acute phase heart failure. The percent reduction of the slope did not correlate with these parameters. In conclusion, a substantial fraction of patients with AMI have excessive ventilation that improves in 4 months. The improvement is greater in patients with greater excessive ventilation but is not associated with an improvement in exercise capacity nor hemodynamics. (Jpn Circ J 2001; 65: 399 - 403)

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The efficacy of anticoagulation in reducing the risk of cardiogenic embolism has been demonstrated in patients with atrial fibrillation (AF), but there are few prospective studies assessing the influence of anticoagulation stability on ischemic stroke in such patients. Accordingly, the present study investigated prospectively whether an instability of the anticoagulation intensity would affect the efficacy of the therapy in a total of 156 patients with non-rheumatic AF (NRAF) who received oral anticoagulation with warfarin. During a 2-year follow-up period, the annual event rate of ischemic stroke was 2.1%. In patients without a history of prior stroke, no ischemic stroke occurred at a higher international normalized ratio (INR ≥2.0). In contrast, patients who had had a prior stroke had no INR-dependent reduction of incidence. The coefficient of variation (CV) of measured INRs was significantly greater in patients with ischemic stroke than in those without. By multivariate analysis, only greater CV (≥0.3) of INRs was an independent risk for ischemic stroke, although New York Heart Association functional class ≥ II and treatment with diuretics were of borderline significance by univariate analysis. The present results suggest that stability of anticoagulation intensity is important to protect thromboembolic events in patients with NRAF. (Jpn Circ J 2001; 65: 404 - 408)

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Previous studies have suggested that aging is associated with progressive arterial stiffness and widening of the pulse pressure, and pulse pressure has been found to be a risk factor of cardiovascular diseases. However, the effects of age, blood pressure (including pulse pressure) or atherogenic factors on thoracic aortic wall stiffness in patients with mild atherosis are unclear, so the present study used transesophageal echocardiography to examine 103 consecutive patients with various cardiovascular diseases. The extent of atherosis was evaluated in terms of intima - medial thickness (IMT), and 2 indices of wall stiffness in the aorta were calculated: elastic modulus and stiffness parameter (β). In subjects with mild atherosis (IMT <1.0 mm), age, body mass index, systolic blood pressure, pulse pressure, triglyceride level, and hypertension were factors significantly associated with high wall stiffness, and multiple logistic stepwise analysis revealed that age, pulse pressure, and triglyceride level were particularly significant. (Jpn Circ J 2001; 65: 409 - 413)

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The present study determined the white blood cell (WBC) count and the serum C-reactive protein (CRP) level in 27 patients with coronary spastic angina, 16 with Braunwald class IB unstable angina (UA) and 13 with Braunwald class IIIB. The relationship between the clinical presentation of UA and the requirement for emergency percutaneous transluminal coronary angioplasty (PTCA) was examined, and in patients with medically refractory angina, the determining factor among the clinical manifestations of angina was also investigated. In the acute phase, the WBC count and the serum CRP level were significantly higher in patients with Braunwald class IIIB than in those with coronary spastic angina or Braunwald class IB UA (p<0.001). In the Braunwald class IIIB group, a significantly higher rate of patients required emergency PTCA than that of the coronary spastic angina group (p<0.01). Patients with medically refractory angina had a significantly higher WBC count and higher serum CRP level on admission, and the WBC count on admission was independently associated with medically refractory angina by multivariate analysis (p<0.05). Inflammation may play a major pathological role in the rapid development of acute coronary syndrome. (Jpn Circ J 2001; 65: 414 - 418)

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The issue of whether exercise training improves exercise hyperpnea in patients after coronary arterial bypass graft (CABG) surgery has not been fully explored. Effects of short-term physical training on ventilatory response and cardiac output during exercise in patients following coronary arterial bypass grafting surgery is studied. Thirty-four patients underwent exercise training for 2 weeks after the second postoperative week (Ex group); 23 stayed sedentary (Sed group). Ventilatory and cardiac output response during the cardiopulmonary exercise test was measured before and after the training period. The minute ventilation - carbon dioxide output (VE-VCO₂) slope decreased from 38.9±8.1 to 35.1±6.7 (p<0.05) in the Ex group, but failed to decrease in the Sed group (39.7±11.1 to 41.5 ±11.4). Cardiac output during exercise at 20 W and at peak exercise, and peak oxygen pulse (VO₂/HR) increased significantly only in the Ex group after training. There was a correlation between improvement of the VE-VCO₂ slope and peak cardiac output during the training interval (r=-0.47) in the Ex group. Short-term physical training after CABG improves ventilatory response to exercise and increases cardiac output during exercise. Improvement of cardiac output is correlated with a decreased value of the VE-VCO₂ slope. (Jpn Circ J 2001; 65: 419 - 423)

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Emergency triage and therapeutic decisions using the recently developed whole blood rapid troponin T test were evaluated and compared with conventional electrocardiographic (ECG) diagnosis in a total of 155 patients with chest pain who visited 16 emergency outpatient clinics in the Tokyo metropolitan area. Thirty-seven patients (23.9%) had a final diagnosis of acute myocardial infarction or high-risk unstable angina requiring emergency coronary intervention and these events were defined as acute coronary syndrome. Diagnostic values using the second-generation rapid troponin T test were evaluated according to 3 time-windows in 85 patients. The sensitivity of the test was 10% for patients assessed within 3 h after the onset, 62.5% for 3-6 h after, and 75% for more than 6 h, whereas conventional ECG diagnosis had 100% sensitivity at any time-window. In contrast, the specificity of the rapid troponin T test was 100%, 100%, and 97.4%, whereas that of conventional ECG diagnosis was 25%, 57.1%, and 42.2%, respectively for the 3 time-windows. The positive predictive value of ECG diagnosis was inferior to the rapid troponin T test, which reflected the prudent attitude of physicians taking ECG decisions as positive when myocardial ischemia was suspected. The diagnostic efficacy of the rapid troponin T test was remarkable in patients with the non-ST elevation type of acute coronary syndrome. A questionnaire survey on therapeutic decisions revealed that only 10% of Tokyo outpatient institutes performed prehospital thrombolytic therapy, 30-33% administered aspirin or nitrate, and 16.7% gave heparin. The rapid troponin T test is extremely useful for cardiac emergency triage and therapeutic decision making. There is a requirement for practical guidelines for the primary therapeutic decisions for patients with suspicious acute coronary syndrome. (Jpn Circ J 2001; 65: 424 - 428)

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This study investigated if specific histological features correlate with remodeling in human coronary arteries treated by balloon angioplasty (PTCA). Segments of perfusion-fixed coronary arteries that had undergone antemortem PTCA were obtained from 15 patients and primary atherosclerotic (CAD) lesions obtained from these hearts were used as control lesions. Arterial segments were serially divided to yield 108 sub-segments for PTCA lesions and 38 sub-segments for CAD lesions. A linear regression analysis was used to determine the relationship between 14 histological parameters and an arbitrary index of compensatory arterial enlargement, the external elastic lamina (EEL) index (EELI), defined as the ratio of the area encompassed by the EEL to the sum of the intimal area (IA) + medial area (MA). In PTCA arteries the abundance of plaque microvessels negatively correlated with the EELI (p=0.04), but in CAD arteries there was no relationship between histology and the EELI. The abundance of plaque microvessels correlates with the magnitude of constriction in coronary artery lesions subjected to PTCA. This study provides descriptive insights into the biology of remodeling in human coronary arteries after angioplasty, and suggests that the endothelium may play an important role. (Jpn Circ J 2001; 65: 429 - 433)

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It has been previously reported that sauna therapy, a thermal therapy, improves the hemodynamics and clinical symptoms in patients with chronic heart failure and also improves endothelial function, which is impaired in such patients. The present study investigated whether the improvements observed with sauna therapy are through modulation of arterial endothelial nitric oxide synthase (eNOS) expression. Eight male Syrian golden hamsters underwent sauna therapy, using an experimental far infrared-ray dry sauna system, at 39°C for 15 min followed by 30°C for 20 min daily for 4 weeks. Control group hamsters were placed in the sauna system switched off at room temperature of 24°C for 35 min. Immunohistochemistry found greater amounts of the immunoreactive products of eNOS in the endothelial cells of the aorta and carotid, femoral and coronary arteries in the sauna group than in the control group. Western blot analysis also revealed that 4-week sauna therapy significantly increased eNOS expression in aortas by 50% in 4 series of independent experiments with an identical protocol (p<0.01). In reverse transcription polymerase chain reaction assay, the eNOS mRNA in aortas was greater in the sauna group than in controls, with a peak at 1-week of sauna therapy (approximately 40-fold increase). In conclusion, repeated thermal therapy upregulates eNOS expression in arterial endothelium. (Jpn Circ J 2001; 65: 434 - 438)

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The present study examined whether basic fibroblast growth factor (bFGF)-impregnated acidic gelatin hydrogel microspheres (AGHM) would enhance collateral development to the infarct area in dogs with coronary occlusion. Studies were conducted in 28 dogs with a 2-week occlusion of the proximal left anterior descending coronary artery (LAD). The dogs were divided into 3 groups according to treatment: Group A treated with bFGF-impregnated AGHM in the infarct area; Group B with free-form bFGF; Group C with AGHM alone. Coronary angiography (n=15; Group A, 7 dogs; Group B, 5 dogs; Group C, 3 dogs) and a regional myocardial blood flow study (n=13; Group A, 6 dogs; Group B, 4 dogs; Group C, 3 dogs) were repeated at a 2-week interval. Coronary angiography revealed that in Group A, antegrade flow in the LAD distal to the occlusion, which was assessed by Thrombolysis in Myocardial Infarction (TIMI) grade, was significantly increased after treatment. In contrast, in Groups B and C, the treatment did not change the flow grade in the LAD. In Group A, the regional myocardial blood flow in the collateral dependent area was significantly increased after treatment, and the regional myocardial blood flow reserve after adenosine injection was also significantly increased. These measurements remained after treatment in Groups B and C. The immunohistochemical study with factor VIII-related antigen revealed an increase of vascular density in the ischemic region in Group A. Intramyocardial delivery of bFGF-impregnated AGHM, but not free-form bFGF, improves the collateral circulation to the infarct area of a coronary occlusion in dogs. (Jpn Circ J 2001; 65: 439 - 444)

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Lumican belongs to the small leucine-rich proteoglycan family and has an important role in the regulation of corneal and dermal collagen fiber assembly. Recently, lumican mRNA was found in the heart and its high expression was reported during wound healing of the cornea. In the present study, the expression and role of lumican in fibrosis of an ischemic and reperfused rat heart were examined. The expression level of lumican mRNA increased in the ischemic and reperfused rat heart and was highest on the fourth week. Lumican protein existed in the forms of core protein and proteoglycan in the control rat heart. The amount of lumican in the form of proteoglycan increased, and that as the form glycoprotein was newly detected in the ischemic and reperfused rat heart on the fourth week. In the control heart, lumican was weakly expressed in the collagen fibers of the perivascular area, but it was expressed strongly in many capillary endothelial cells in the ischemic lesion on day 1. After 3 days, lumican was localized in collagen fibers and in the fibroblasts of fibrotic lesions. A few myocardial cells close to the ischemic lesion expressed lumican mRNA. Lumican is considered to play an important role in the fibrillogenesis of the ischemic and reperfused rat heart. (Jpn Circ J 2001; 65: 445 - 450)

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The role of cardiac adenosine triphosphate-sensitive K⁺ (K_ATP) channels induced by angiotensin II type 1 (AT1) receptor antagonist, CV-11974, on myocardial metabolism and contraction during ischemia, and reperfusion by the phosphorus 31-nuclear magnetic resonance in Langendorff-perfused rabbit hearts was investigated. After 20 min of continuous normothermic global ischemia, 30 min of postischemic reperfusion was carried out. CV-11974 with or without the K_ATP channel blocker, glibenclamide, or the bradykinin B₂ receptor antagonist, _D-Arg-[Hyp ³,_D-Phe⁷]bradykinin, was administered 40 min prior to the global ischemia. Adenosine triphosphate (ATP), creatine phosphate (PCr), inorganic phosphate (Pi), intracellular pH (pHi), left ventricular systolic developed pressure, left ventricular end-diastolic pressure (LVEDP), and coronary flow were measured. Twenty-eight hearts were divided into 4 experimental groups consisting of 7 hearts each. Group I consisted of controls, Group II perfused with CV-11974 (10^-6 mol/L), Group III perfused with CV-11974 (10 ^-6 mol/L) in combination with glibenclamide (10^-6 mol/L), and Group IV perfused with CV-11974 (10^-6 mol/L) in combination with _D-Arg-[Hyp³,_D-Phe ⁷]bradykinin (10^-6 mol/L). Group II showed a significant inhibition of the decrease in ATP during ischemia and reperfusion compared with Group I (p<0.01), being 42±3% and 19±4% at ischemia, 69±3% and 47±4% at reperfusion in Group II and Group I, respectively. Group II also showed a significant inhibition of the increase in LVEDP during ischemia and reperfusion compared with Group I (p<0.01), being 13±4 mmHg and 52±8 mmHg at ischemia, 8±2 mmHg and 26±5 mmHg at reperfusion in Group II and Group I, respectively. However, Group III did not inhibit the decrease in ATP and the increase in LVEDP during ischemia and reperfusion. Group IV also showed no inhibition of the aforementioned parameters during the same period. These results suggest that CV-11974 has a significant beneficial effect for improving myocardial energy metabolism and relaxation during both myocardial ischemia and reperfusion, which is provided by K_ATP channels and bradykinin B₂ receptor. The cardioprotective quality of the AT1 receptor antagonist is caused by the K_ATP channels that are mediated by the bradykinin B₂ receptor. (Jpn Circ J 2001; 65: 451 - 456)

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The present study aimed to identify the patency achieved by a bi-directional Glenn shunt procedure by shaded volume rendering (VR) images using electron-beam computed tomography (EBCT). A Damus Kay-Stanzel type procedure was performed on a female with hypoplastic left heart syndrome who later received a bi-directional Glenn shunt to increase pulmonary blood flow. In considering the characteristics of the bi-directional Glenn shunt procedure, in which the superior vena cava is connected to the right pulmonary artery, an early phase acquisition protocol with injection of contrast material from the right cubital vein using the step volume scan mode of EBCT was planned to acquire blood flow information. Excellent spatial resolution volume data of the heart and great vessels was obtained from which 3-dimensional images were made. Bi-directional Glenn shunt flow could be observed directly and the complex morphology and relationships between adjacent structures were revealed by 3-dimensional VR imaging. The combination of EBCT and VR can provide useful information to evaluate congenital heart diseases. (Jpn Circ J 2001; 65: 457 - 461)

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Glycogen storage disease (GSD) types II, III, IV, and V may be associated with cardiomyopathy, but, with the exception of type III GSD, adult cases are extremely rare. A 62-year-old man was found to have GSD and a concomitant left ventricular aneurysm. He had been comparatively well until the age of 62 years, although he had suffered a cerebral infarction at the age of 35 years. The damage caused by glycogen deposition was strictly confined to the myocardium. Left ventriculography revealed a left ventricular aneurysm in the apex. The serial change on electrocardiogram, as well as the findings of the echocardiogram and of cardiac catheterization, resembled those of the dilated phase of hypertrophic cardiomyopathy. However, a left ventricular endomyocardial biopsy specimen revealed central vacuolar degeneration of myocytes with depositions of glycogen. The GSD type remains unknown in the present patient, because the activity of debranching enzyme (type III) measured from the skeletal muscle specimen was normal, whereas that of acid maltase (type II) was slightly low. It is possible that there is a specific malfunction of the acid maltase of the myocardium in the present patient. (Jpn Circ J 2001; 65: 462 - 464)

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A 25-year-old Japanese female complaining chest oppression and palpitation was admitted to hospital under the presumptive diagnosis of ischemic heart disease (IHD), although no obvious underlying disease associated with IHD was detected. Coronary angiography showed stenosis at the proximal site of left anterior descending artery (LAD), with dilatation and tortuosity at the bifurcation of the first and the second septal branches. Intravascular ultrasound imaging of the LAD showed intimal thickness without calcification at the site of stenosis. The stenosis was successfully and smoothly dilated by percutaneous transluminal angioplasty. Even with precise evaluation, the cause of the coronary artery disease in this young female patient was not clarified. Further careful follow-up is needed. (Jpn Circ J 2001; 65: 465 - 467)

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An implantable cardioverter defibrillator (ICD) was used in a 62-year-old man with dilated cardiomyopathy (DCM) because of hemodynamically intolerable ventricular tachycardia (VT). Amiodarone was administered after a second episode of ICD discharge. Three weeks later, incessant VT appeared, and DC discharge failed to terminate it. Microvolt T wave alternans (TWA), measured by a spectral method, was observed in this patient with and without amiodarone administration. The onset heart rate with TWA was lower and the alternans voltage was higher with amiodarone than without it. The effects of amiodarone appeared to be related to the exacerbation of VT and an increased defibrillation threshold. TWA might be useful in predicting the proarrhythmic effects of amiodarone in similar cases. (Jpn Circ J 2001; 65: 468 - 470)

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A 30-year-old man was diagnosed to have an anomalous origin of the right coronary from the pulmonary artery. Through a mini-sternotomy, without extracorporeal circulation, reimplantation of the anomalous origin of the right coronary artery from the pulmonary artery to the aorta was successfully performed. This is a successful case of off-pump cardiac correction of this type of isolated anomaly, using a minimally invasive approach. (Jpn Circ J 2001; 65: 471 - 472)

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